AKT1 and neoplasm: The exon 11 codons 557/558 deletions may perturb KIT kinase autoinhibition by controlling the a-helical conformation, essentially leading to increased spontaneous receptor phosphorylation, the activation of Ras/Raf/MAPK, JAK/STAT3 and PI3K/Akt/mTOR downstream signaling pathways, ultimately leading tumor cell proliferation and the inhibition of apoptosis [36].